Our recent findings have established that functional connectivity exists in the visual centers of the adult anophthalmic mouse despite the total absence of retinal afferent fibers. We have previously demonstrated that the retinal afferents are replaced by large terminals in the dLGN in the anophthalmic mouse. Moreover, we have demonstrated experimentally that these replacement terminals have a subcortical origin. Another plastic response in the anophthalmic mouse involves a greater than normal extrageniculate thalamocortical projection to area 17 that arises from the nucleus lateralis posterior. It is evident that our next effort should be directed to prenatal differentiation of the visual centers in anophthalmic and normal mice. A systematic analysis of ontogenesis of the dLGN is being initiated which involves morphometry at the light and electron microscopic levels. The collection of timed stages of embryonic development will be enlarged and standardized technically. Besides this classic approach, we have begun to perform intrauterine enucleation of normal embryos from days 13-19 in an effort to determine more directly what the anatomic and physiologic consequences of primary deafferentation in utero will be in a control animal equipped with the genome for normal vision. Our initial success with this difficult surgery holds promise of our obtaining a valid normal control preparation for the anophthalmic mutant mouse.